In rats infected with the cestode Taenia taeniaeformis, hepatomegaly results from development of parasitic cysts in the liver. Diffuse nodular mucosal hyperplasia in the glandular region (corpus and antrum) of the stomach, and gross thickening of the intestinal mucosa also result. Between postinfection days (PID) 21 and 84, radiologic observations were made after oral administration of a barium sulfate suspension in T taeniaeformis-infected rats and in age/sex-matched controls. There was radiographic evidence of hepatic enlargement at PID 21. Enlargement of the gastric folds was first observed along the greater curvature of the stomach at PID 35. Fimbriation of small intestinal mucosal surfaces resulted from thickening of the intestinal villi and was observed in the duodenum at PID 21. Intestinal motility was assessed, and contractions were counted, using image intensification fluoroscopy, then were recorded on videotape. There were no significant differences between control and infected rats for gastric emptying time, intestinal transit time, and number of intestinal contractions per minute. Barium contrast radiography clearly indicated large gastric folds, thickening of the small intestinal villi, and hepatic enlargement, and was useful for assessing gastrointestinal motility.

Cardiopulmonary consequences of IV administered glycopyrrolate (0.01 mg/kg of body weight), followed in 11 +/- 2 minutes by butorphanol (0.2 mg/ kg) and xylazine (0.5 mg/kg), were evaluated in 6 dogs, with and without nasal administration of oxygen (100 ml/kg/min). Glycopyrrolate caused significant (P < 0.05) increases in heart rate and cardiac index and significant (P < 0.05) decreases in stroke index. Subsequent administration of butorphanol and xylazine was associated with significant (P < 0.05) increases in systemic vascular resistance, mean arterial blood pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, PaCO2, venous admixture, oxygen extraction ratio, and hemoglobin concentration. It caused significant (P < 0.05) decreases in cardiac index, stroke index, breathing rate, minute volume index, oxygen delivery, and oxygen consumption. Mean arterial blood pressure, pulmonary vascular resistance, tidal volume index, and minute volume index were significantly (P < 0.05) higher when dogs were breathing room air. The arterial and venous PO2, and PCO2, and venous oxygen content were significantly (P < 0.05) higher, and the arterial and venous pH, and oxygen consumption were significantly (P < 0.05) lower when oxygen was administered. Pulsus alternans and S-T segment depression were observed in dogs of both groups. Ventricular premature contractions were observed in 1 dog breathing room air. All dogs were intubated briefly 15 minutes after administration of butorphanol and xylazine. Time to first spontaneous movement was 45 minutes. All dogs remained in lateral recumbency without physical restraint for 60 minutes.

The effect of mimicking prepartum concentration of estradiol-17 beta on the inflammatory response to endotoxin in gilts was studied. The study was performed in a split-litter design and comprised 5 pairs of littermates. A catheter was inserted into the jugular vein 2 days prior to the start of the study. In each pair, 1 littermate was treated IM with 2.5 mg of estradiol-17 beta/75 kg of body weight, and the other littermate was given peanut oil IM as a control. The day after treatment, all gilts were challenge-exposed with a Salmonella typhimurium-derived endotoxin (1 microgram/kg, IV) and the inflammatory response to challenge exposure was monitored. There was no effect of estradiol treatment on the transient clinical signs of endotoxemia or on the increase in rectal temperature. The increase in blood concentrations of prostaglandin F2 alpha, metabolite and cortisol after endotoxin challenge exposure was not affected by estradiol. Decrease in number of circulating blood mononuclear cells and polymorphonuclear leukocytes was not changed by estradiol treatment. Taken together, mimicking prepartum concentration of estradiol did not affect either the magnitude or the kinetics of the inflammatory response to endotoxin in gilts. Relevance of these findings to development of endotoxin-mediated diseases, such as the postpartum agalactia syndrome, needs further study.

Generation of free radicals and the ability of various antioxidants to attenuate radical production in freshly procured cancellous bone specimens was investigated, using spin-trapping and electron spin resonance (ESR) techniques. Seven core cancellous bone specimens, 10 mm long and 7.9 mm in diameter, were obtained using aseptic technique, from the proximal portion of the humerus of 9 adult mixed-breed dogs. One core cancellous bone specimen from each dog was incubated in spin trap alpha-phenyl-N-tert-butylnitrone in Eagle's minimum essential medium and served as a control. The other 6 specimens from each dog were incubated in alpha-phenyl-N-tert-butylnitrone/Eagle's minimum essential medium plus 1 of the following antioxidants: superoxide dismutase, catalase, superoxide dismutase/catalase, indomethacin, allopurinol, or deferoxamine mesylate. All specimens were incubated at 26 C for 90 minutes, then frozen at -20 C until they were prepared for analysis by ESR spectroscopy. Each specimen was thawed, homogenized, and extracted in a low-dielectric organic solvent prior to obtaining an ESR spectrum which was analyzed for hyperfine splitting constants to identify radicals. Each first-derivative spectrum was digitally double-integrated to obtain an area: these areas were used to compare intensities of the spin. For each treatment group, the areas from the treated specimens were compared with the areas from the control specimens, using a paired t-test. Significance was accepted at P less than or equal to 0.05. Spin adducts were detected in all cancellous bone specimens. Specimens incubated in deferoxamine (P = 0.0017) and superoxide dismutase/catalase (P = 0.0452) had significantly smaller areas than did control specimens. The areas for the other treatment groups did not differ significantly from controls. Our results substantiate free radical production in freshly procured cancellous bone specimens and that radical formation is attenuated by in vitro incubation with deferoxamine or superoxide dismutase/catalase.

Effects of differential ventilation on gas exchange were studied in 7 isoflurane-anesthetized, laterally recumbent horses, and were compared with effects of conventional ventilation, using similar minute volume. A tracheal tube-in-tube intubation technique allowed each lung to be connected separately to an anesthetic circle system with a ventilator. Two distribution patterns of tidal volume were investigated; half the tidal volume was distributed to each lung and two-thirds the tidal volume was distributed to the dependent lung. Effects of the combination of these patterns with positive end-expiratory pressure (PEEP) of 10 and 20 cm of H20 to the dependent lung were investigated. Differential ventilation maintained PaCO2, but significantly increased PaO2, from 180 to 270 mm of Hg (+44%) and decreased shunt perfusion from 22 to 19% (-15%), regardless of the distribution pattern used. Mean airway pressure was lower than the value detected during conventional ventilation. The combination of differential ventilation with selective PEEP was followed by a decrease in PaCO2 and further increase of PaO2 and decrease of shunt, which were similar for both distribution patterns. Effects of PEEP of 20 cm of H2O were more pronounced than those of PEEP of 10 cm of H2O. Owing to the combined effects of differential ventilation and selective PEEP, PaO2 increased to 399 mm of Hg and shunt decreased to 15%. This represents increase of 112% and decrease of 33% respectively, compared with values for conventional ventilation. Mean airway pressure increased maximally to 23 cm of H2O, which was 11 cm of H2O greater than the value for conventional ventilation. During differential ventilation, alveolar dead space in the dependent lung became greater than that in the nondependent lung and maximum was 39%. There were no significant changes in arterial blood pressure. Beneficial effects on gas exchange can be explained by improved matching of ventilation and perfusion, possibly attributable to reopening of previously dosed units in the dependent lung.

Once daily for 3 days, laser Doppler flowmetry was used in 5 healthy, nonsedated adult horses to evaluate coronary band and laminar microcirculatory blood flow (MBF) in both forelimbs, The coronary band had significantly (P < 0.05) higher MBF than did the laminae on the days evaluated. Significant variation in MBF was not found over the 3-day measurement period in any one site. Significant (P < 0.05) variation was found in coronary band MBF among horses. This variation was not observed in laminar MBF. On occlusion of the digital arteries at the level of the fetlock, marked decrease in coronary band and laminar MBF was observed. Twenty minutes after IV administration of acetylpromazine, marked increase in coronary band and laminar MBF was observed. The technique was easily performed in standing nonsedated horses, did not inflict discomfort, lacked complications, and measurements were repeatable. This technique provides an index of digital MBF, either intermittently or continuously, avoiding introduction of invasive variables associated with other techniques.

Cell-mediated immunity was evaluated in intestinal, respiratory, and systemic lymphoid tissues of pigs exposed when 11 days old to virulent transmissible gastroenteritis virus (TGEV), attenuated TGEV, or porcine respiratory coronavirus (PRCV), 3 antigenically related porcine coronaviruses with distinct enteric and respiratory tissue tropisms. Mononuclear cells were prepared from mesenteric lymph nodes (MLN), bronchial lymph nodes (BLN), and spleens of pigs and tested for virus-specific responses by use of lymphocyte proliferation assays. Vigorous MLN and BLN proliferation responses to virulent TGEV and PRCV, respectively, at postinoculation days 8 to 24 were strongly associated with prior detection of TGEV in rectal swab samples and PRCV in nasal swab samples. Gastrointestinal disease and intestinal virus replication, assessed on the basis of rectal virus shedding, were almost exclusively found in the virulent TGEV-inoculated pigs, even though virulent TGEV and a high dose of attenuated TGEV elicited the highest proliferation responses in MLN. Pigs exposed to PRCV or attenuated TGEV did not have clinical signs of disease, and only 1 pig given a high dose of attenuated TGEV shed virus in feces. Porcine respiratory coronavirus replicated in the respiratory tract after either oronasal or aerosol inoculation of virus and induced strong BLN, but not MLN, proliferation responses. A high dose of attenuated TGEV (4 X 10(8) plaque-forming units) was more effective than a lower dose of attenuated TGEV (7 X 10(6) plaque-forming units) in eliciting significant lymphocyte proliferation in MLN and BLN. Cellular immune function, assessed on the basis of mitogen-induced proliferation of lymphocytes, was comparable for all 3 sources of lymphocytes and was not adversely affected by exposure to any of the pigs. The tissue tropism of TGEV and PRCV was associated with induction of virus-specific cell-mediated immune responses, as evidenced by substantial lymphocyte proliferation responses in MLN and BLN, mucosa-associated lymph nodes adjacent to the primary sites of virus replication. The failure of PRCV strain ISU-1 to replicate in the intestinal tract correlated with poor virus-specific cellular immune responses in MLN.

The main objective of the study reported here was to generate a panel of monoclonal antibodies (MAB) to bovine neutrophil surface antigens, and to identify MAB that modulate neutrophil chemotaxis, respiratory burst, and phagocytosis. A further objective was to study MAB reactivity with resting and activated neutrophils, to identify activation antigens and adhesion molecules. A panel of 14 MAB was generated by producing murine hybridomas. Neutrophils incubated with MAB at 4 C for 2 hours were used in chemotaxis, respiratory burst, and phagocytosis assays. Chemotaxis was evaluated in Boyden chambers, using Escherichia coli endotoxin-activated fetal bovine serum as the chemoattractant. Respiratory burst was determined by measuring chemoluminescence of neutrophils incubated with 5-amino-2,3-dihydro-1,4-phthalazinedione, and serum opsonized zymosan. Phagocytosis was determined by flow cytometry, using fluorescein-labeled Staphylococcus aureus. The MAB S7G8, S5F8G10, S7E10, and S5F8B8 enhanced chemotaxis (to > 125% of control). The MAB S7E10 and S8D9 enhanced respiratory burst activity (to > 125% of control), whereas MAB S2G8, S4G10, S8G10, and S5F8B8 caused inhibition (to < 75% of control). The MAB S2G8, S4G10, S8G10, and S5F8G10 enhanced phagocytosis (to > 125% of control). Chemotaxis, respiratory burst, and phagocytosis values of neutrophils not bound with MAB served as controls for comparison. The MAB binding for nonactivated neutrophils (at 4 C) ranged from 9 to 100%, and for activated neutrophils (at 37 C; at 37 C with phorbol myristate acetate) from 90 to 100%. Binding of MAB S4F5, S5F8B8, S6C6, S7E10, S8D9, and S5F8G10 increased when neutrophils had been incubated at 37 C. Binding of these MAB was further increased after incubation with phorbol myristate acetate (100 ng/ml) at 37 C, indicating recognition of activation antigens by MAB. The MAB generated in this study appeared to be potential candidates for studying mechanisms of neutrophil function and for enhancing neutrophil function in vitro and in vivo.

4-Methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (EG) intoxication. Eleven dogs were given 10.6 g of EG/kg of body weight; 5 dogs were treated with 4-MP 5 hours after EG ingestion and 6 dogs were treated with 4-MP 8 hours after EG ingestion. 4-Methylpyrazole was administered IV as a 50-mg/dl solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/ kg; at 24 hours after initial dose, 10 mg/kg, and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after EG ingestion. Dogs of both groups developed clinicopathologic signs associated with EG intoxication, including CNS depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after EG ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after EG ingestion that developed acute renal failure. All dogs treated 5 hours after EG ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after EG ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after EG ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment. Of the dogs treated 8 hours after EG ingestion, 3 recovered without morphologic, biochemical, or clinical evidence of renal impairment. Serum half-life of EG was prolonged in the dogs treated 8 hours after EG ingestion. Percentage of EG excreted unchanged was 84 +/- 2% in the dogs treated 5 hours after EG ingestion, and was 40 +/- 10% in the dogs treated 8 hours after EG ingestion. 4-Methylpyrazole was effective in preventing renal failure in all dogs given 10.6 g of EG/kg when treatment was initiated by 5 hours after EG ingestion, and in 4 of 6 dogs when treatment was initiated by 8 hours after EG ingestion.

Force plate gait analysis was used to study the effects of subject stance time and velocity on ground reaction forces in 5 adult Greyhounds at the walk. Data from 146 valid trials were obtained. Stance time and velocity were linearly related, and stance time had a strong, negative correlation with velocity k = -0.72 for the forelimbs, r = -0.56 for the hind limbs). Stance time correlated more closely with changes in peak vertical force and impulse than did velocity. Stance time and velocity correlated less strongly with braking and propulsion forces and impulses. The trials were divided into 2 distinct velocity ranges (V1 = 0.92 to 1.03 m/s, V2 = 1.06 to 1.17 m/ s), 2 distinct forelimb stance time ranges (FST1 = 0.43 to 0.48 second, FST2 = 0.50 to 0.55 second), and 2 distinct hind limb stance time ranges (HST1 = 0.40 to 0.45 second, HST2 = 0.46 to 0.51 second). Five trials from each dog were included in each range, and the mean values were used to evaluate changes in ground reaction forces between groups. Peak vertical force in the forelimbs decreased significantly (P = 0.048) as FST increased; however, difference was not detected in vertical force between velocity groups. Peak vertical force in the hind limbs decreased significantly (P = 0.001) as HST increased and increased significantly (P = 0.000) as velocity increased. Differences were not observed between groups in forelimb or hind limb braking and propulsive forces. Vertical impulse in the forelimbs and hind limbs decreased as velocity increased and increased as stance time increased. Braking impulse in the forelimbs decreased as velocity increased and increased as FST increased. Braking force in the hind limbs did not change between velocity or stance time groups. Propulsive impulse in the hind limbs decreased as velocity increased and increased as HST increased. Stance time was a sensitive and accurate indicator of subject velocity in clinically normal dogs at the walk and correlated more closely with changes in some ground reaction forces than did velocity measurements. Stance time measurements could be used to normalize trial data within a sampling period and document consistency in velocity during force plate analysis of clinically normal dogs at the walk.